Rapid fall in circulating non‐classical monocytes in ST elevation myocardial infarction patients correlates with cardiac injury

• Published in: The FASEB journal Vol. 35; no. 5; pp. e21604 - n/a
• Main Authors: Marsh, Sarah A., Park, Catherine, Redgrave, Rachael E., Singh, Esha, Draganova, Lilia, Boag, Stephen E., Spray, Luke, Ali, Simi, Spyridopoulos, Ioakim, Arthur, Helen M.
• Format: Journal Article
• Language: English
• Published: United States 01.05.2021
• Subjects: animal models; Animals; coronary circulation; Female; Heart Injuries - blood; Heart Injuries - etiology; Heart Injuries - pathology; Humans; Male; Mice; Middle Aged; monocytes; Monocytes - pathology; myocardial infarction; Prospective Studies; Retrospective Studies; ST Elevation Myocardial Infarction - complications; coronary circulation; monocytes; animal models; myocardial infarction
• DOI: 10.1096/fj.202100240R
• ISSN: 0892-6638

Myocardial infarction leads to a rapid innate immune response that is ultimately required for repair of damaged heart tissue. We therefore examined circulating monocyte dynamics immediately after reperfusion of the culprit coronary vessel in STEMI patients to determine whether this correlated with level of cardiac injury. A mouse model of cardiac ischemia/reperfusion injury was subsequently used to establish the degree of monocyte margination to the coronary vasculature that could potentially contribute to the drop in circulating monocytes. We retrospectively analyzed blood samples from 51 STEMI patients to assess the number of non‐classical (NC), classical, and intermediate monocytes immediately following primary percutaneous coronary intervention. Classical and intermediate monocytes showed minimal change. On the other hand, circulating numbers of NC monocytes fell by approximately 50% at 90 minutes post‐reperfusion. This rapid decrease in NC monocytes was greatest in patients with the largest infarct size (P < .05) and correlated inversely with left ventricular function (r = 0.41, P = .04). The early fall in NC monocytes post‐reperfusion was confirmed in a second prospective study of 13 STEMI patients. Furthermore, in a mouse cardiac ischemia model, there was significant monocyte adhesion to coronary vessel endothelium at 2 hours post‐reperfusion pointing to a specific and rapid vessel margination response to cardiac injury. In conclusion, rapid depletion of NC monocytes from the circulation in STEMI patients following coronary artery reperfusion correlates with the level of acute cardiac injury and involves rapid margination to the coronary vasculature.